A New Monitor of Pressure Autoregulation: What Does It Add?

Abstract

Cerebrovascular pressure autoregulation is a vital, protective mechanism that constrains cerebral blood flow during changes in arterial blood pressure. Pressure autoregulation is known to fail during profound hypotension, and the so-called lower limit of autoregulation (LLA) is diverse for different subjects. 1 The measurement and monitoring of pressure autoregulation is specifically useful to discriminate safe from harmful blood pressure: when arterial blood pressure is within range to render normal pressure autoregulation measurements, the brain is protected; when arterial blood pressure is too low and pressure autoregulation measurements show impairment, the brain is vulnerable. 2,3 In the present study, Hori et al. 4 present a novel method to measure pressure autoregulation using the Ornim UT-light technology (Ornim, Inc., Kfar Saba, Israel), rendered as a cerebral flow velocity index (CFVx). The UT-light method is proprietary and quantifies relative tissue blood movement from the Doppler shift of near-infrared light caused by red cells in motion. It is an uncalibrated, surrogate measure of cerebral blood flow. How does this measure autoregulation? How is this to be evaluated and validated? Not fewer than 15 metrics purported to measure autoregulation have infused the medical literature within hundreds of manuscripts in the past 2 decades. 5 It would be instructive to know how these metrics are related and to consider the evidentiary burden required to deploy them clinically. Pressure autoregulation is distinct from, but often confused with, other servomechanisms that contribute to the homeostasis of cerebral blood flow. Examples include neurovascular coupling (or metabolic autoregulation), which rapidly matches cerebral blood flow to local metabolic demands 6 ; the systemic vasoconstrictive response to shock, which diverts cardiac output from sympathetic, angiotensin, and vasopressin-reactive vascular beds to the brain and heart, which respond differently to these neurohormonal cues 7–9 ; and cerebral vasodilatory and constrictive responses caused by changes in arterial carbon dioxide. 10 Each of these operates at the same point of action, that is to affect a change or to prevent a change in cerebral blood flow. The pressure autoregulation mechanism can be measured even when cerebral blood flow is influenced by the other mechanisms listed if the metric used is attuned to the proper frequency. Three components are needed to construct a metric of autoregulation: